Monthly Archives: May 2011

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A large white butterfly caterpillar weaves a cocoon around the wasp larvae infesting its body. Photo by EntomoAgricola.

I’m embarrassed to admit that I’ve only just gotten around to picking up Carl Zimmer’s book Parasite Rex. It’s turned out to be a wonderful compendium of all the peculiar ways parasites evade, confound, and resist the defenses of their hosts. Some of the wildest cases Zimmer examines, though, are parasites that manipulate their hosts’ behavior.

One grotesque and well-studied example is the wasp Cotesia glomerata. Female C. glomerata wasps inject their eggs into butterfly caterpillars, and when the eggs hatch, the wasp larvae eat the caterpillar from the inside, saving critical organs so the poor thing stays alive the whole time. Then, when the wasp larvae are ready to burrow out of the caterpillar and form pupae to complete their devlopment, they induce the half-dead caterpillar to spin a web around them and stand guard against predators. (In technical language, this life history makes the wasp a parasitoid, rather than a parasite.) Christie Wilcox has written up a fuller description of the whole grisly process, if you want more detail.

That sounds like a pretty incredible set of manipulations for one clutch of wormy-looking wasp larvae, but they’re not all that Cotesia glomerata can do. New evidence published in Ecology Letters suggests that C. glomerata can somehow make the plants that its host caterpillar feeds on less hospitable [$a] to the larvae of another caterpillar-infesting wasp. In other words, the wasp larvae may manipulate not just their host, but their host’s host.

First off, here’s video of Cotesia glomerata in action. Don’t watch this on your lunch break.

Now, the wasp’s plant manipulations. Lots of plants have what are called induced defenses against herbivores like the butterfly larvae that host C. glomerata larvae. Induced defenses are usually protective toxins that plants produce in response to herbivore damage [PDF]. Erik Poelman and his collaborators reasoned that, since C. glomerata can manipulate it’s host’s behavior, the parasites might change how plants respond to herbivory by infested caterpillars.

To test this, the team first had to induce plant responses. They grew Brassica oleracea—Brussels sprouts—plants in the greenhouse, then infested them with either un-parasitized caterpillars of the cabbage white butterfly Pieris rapae, cabbage white caterpillars infected with Cotesia glomerata, or cabbage white caterpillars infected with larvae of the related wasp C. rubecula. Once the caterpillars had nibbled on the plants enough to induce defensive responses, Poelman et al. removed the caterpillars in preparation for the experiment proper.

The team then introduced parasitoid-free caterpillars and caterpillars infested with one or the other parasitoid species onto host plants that had been through one of the three induction treatments, or that had never been exposed to herbivores. They then tracked the development of the caterpillars, and whether or not the wasp larvae inside them survived.

Larvae of C. rubecula fared more-or-less equally well no matter what kind of plant their host caterpillar fed on. But C. glomerata larvae had substantially higher mortality when their hosts fed on plants induced by caterpillars infested with the competitor species. While about 50 percent of C. glomerata larvae died if their hosts fed on plants induced by uninfested caterpillars or caterpillars infested with C. glomerata, almost 75 percent of C. glomerata larvae died when their hosts fed on plants that had previously been occupied by caterpillars infested with C. rubecula.

This impact isn’t because the host caterpillars fared poorly—in fact, caterpillars developed a little faster on plants induced by rubecula-infested caterpillars. So somehow, Cotesia rubecula seems to have influenced its hosts in a way that makes their host plants less hospitable to C. glomerata.

Poelman et al. are scrupulous to point out that this effect might not be anywhere nearly as strong in nature—host plants and host caterpillars might be plentiful enough that Cotesia glomerata can simply avoid the competitor species. On top of that, any natural selection that C. rubecula could be exerting on C. glomerata via induced responses in their shared hosts’ host plants is occurring at multiple removes. The effect Poelman et al. documented is probably not an adaptation for competition with C. glomerata so much as a side effect of C. rubecula‘s effect on its host.

So although this result shows that one parasitoid wasp can reach out and influence another through three other organisms—its own host, that host’s host plant, and the other wasp’s host—it’s not clear how strong that impact has been over the evolutionary history of these two Cotesia species. That said, this is a pretty nifty proof-of-concept.

When Daphnia evolve resistance to pesticides, they become more vulnerable to bacterial parasites. Photo by Chantal Wagner.

If you haven’t read Joseph Heller’s classic Catch-22, cancel your plans for next weekend and spend the time with a copy from the nearest library. It’s a hilarious, bracingly bleak satire of military bureaucracy, as epitomized in the titular clause governing when bomber pilots can be grounded for reason of insanity:

There was only one catch and that was Catch-22, which specified that a concern for one’s safety in the face of dangers that were real and immediate was the process of a rational mind. Orr was crazy and could be grounded. All he had to do was ask; and as soon as he did, he would no longer be crazy and would have to fly more missions.

Heller conceived Catch-22 as a product of malicious middle management, but a similar situation crops up in the natural world when living things are under natural selection from conditions that favor contradictory traits. Biologists most commonly call these tradeoffs.

Over the course of evolution, tradeoffs set up “choices” that natural selection must make—a population can adapt to one alternative set of conditions, or another, or settle on a middle ground. A trivial example is that elephants have long ago “chosen” not to fly (Dumbo notwithstanding) in the course of evolving large, un-aerodynamic bodies suitable for massive-scale herbivory. A more relevant example is a new finding that the evolution of pesticide resistance creates vulnerability to parasites [$a].

The US Environmental Protection Agency estimated [PDF] that in 2006 and 2007 (the latest years for which reports are online) we used upwards of five billion pounds of pesticides to kill unwanted plants, insects, fungi, and other organisms worldwide. Once they’re sprayed, we don’t have much control over where pesticides end up—rain runoff takes them into lakes, ponds, and the ocean. In those bodies of water, critters at the base of the food chain are the first to feel the effects—critters like the tiny, translucent crustacean Daphnia magna.

Of course, those critters may be able to evolve resistance to the pesticides contaminating their environment—but that resistance may come at a cost.

Anja Coors and Luc De Meester had already found a hint of this cost [$a] in an experiment using a single clonal line of Daphnia, in which Daphnia exposed to both sublethal concentrations of the widely-used insecticide carbaryl and a parasitic bacterium fared much worse than Daphnia exposed to only carbaryl or bacteria.

In the new study, Coors, De Meester, and three collaborators expand on that initial observation by determining whether Daphnia become more vulnerable to parasites as they evolve resistance to carbaryl, and whether this costly evolution could occur in natural populations. The coauthors took samples of Daphnia from natural populations in four separate lakes and exposed them to carbaryl over several generations—then sampled the resultant evolved populations and tested their vulnerability to the bacterium. Compared to Daphnia left unexposed to carbaryl, the evolved populations were more resistant to the pesticide—and were also more badly hurt by bacterial infection.

It’s hard to say how general this particular result is to the many, many other species that, like Daphnia, must cope with pesticides and other pollutants humans have introduced into the environment. Evolution to resist one pesticide leads to lowered resistance to infection in one aquatic crustacean; in other species, facing different chemicals, maybe such costs are different or lesser or nonexistent. But living things are not infinitely pliable as they evolve in response to the many and rapid changes we’re making in the world. To slow the extinction crisis going on around us, we need to avoid trapping other living things in Catch-22.

So now sending in your posts—new for June or years old—is as easy as copying a permanent URL into the form (preferably in the “message” box) and signing it with your e-mail address. What are you waiting for? [Edited to add:] You have until Monday, 27 June to submit, so I can put the carnival online by the 30th!

The rest of my week is going to consist of driving across two time zones, seeing my parents off on a flight further east with many thanks for their assistance in getting me across those aforementioned timezones, and intensive apartment hunting in not one but two new cities. So no new science post this week; we’ll see how next week goes.

Following up on The Advocate’s declaration that Minneapolis (soon to be one of my two new hometowns), is the gayest city in America, a Daily Show investigation compares Minneapolis to the San Francisco to determine whether the new gay is Minnesota nice. I must admit, banana bread is more my speed, although I’m not so sure about patronizing Target.

Don’t watch unless you don’t mind and/or want to see Jason Jones in a, um, compromising position. Not just shopping at Target, either.

Updated, Friday 13 May: Added a suggested topic and a link to the “recent NAS report.”

June is Pride Month in the U.S., and I’m proud to be joining Alberto Roca of Minority Postdoc to commemorate the month with a blog carnival. On 30 June, Denim and Tweed will host a new entry in the Diversity in Science blog carnival, collecting posts about sexual minorities in the sciences, the science of sexual minorities, and more. For Coming Out Day last October, Steve Silberman and Maggie Koerth-Baker did a fantastic job bringing together the stories of lesbian, gay, bisexual, and transgendered scientists and engineers—Alberto and I are hoping to build on and extend that theme.

GLBT folks and allies who work in the sciences or write about science are invited to submit new posts as well as relevant pieces from their archives. We don’t have a Blog Carnivals submission page online yet (Alberto is working on reviving the DIS page), but you can send links with background information to me at the Denim and Tweed e-mail account—just put “Pride Month blog carnival” in the subject line. Please submit by Monday, 27 June to give me time to put together the carnival post.

Specific topics unique to the LGBT community including gender identity and expression

Coming to terms with being a minority in a majority environment

Again, while we’re hoping to prompt new writing on these topics, we’re also delighted to have folks contribute previously posted work. Please send links to specific posts, and include any information you think might be helpful for me to introduce your contribution.

Beneficial mutations, according to Hollywood, include the superpowered ability to make San Francisco Bay foggy. Photo via Comics Contiuum.

Every time a cell divides is an opportunity for mutation, creating new genetic variation that may be beneficial, may be harmful, or may make no difference at all. In sexually reproducing species, the fate of a useful new mutation is relatively straightforward. If it overcomes the vicissitudes of genetic drift, the mutation will spread through the population as recombination swaps it into different genetic backgrounds, so that on average the mutation spreads or disappears on its own merits.

In asexual species, though, things are less straightforward. This is because new mutations are stuck with the genetic backgrounds in which they first appear—whether they spread of disappear depends not only on the fitness benefits they might provide, but on how beneficial the variation in the rest of the genome is, too. A new beneficial mutation in an asexual population is like a race car driver who can’t change cars—she might be an ace at the wheel, but if she’s stuck in a Yugo, she’s probably not going to win.

So what happens to a new beneficial mutation in an asexual population is largely dependent on random factors: genetic drift and mutation. That randomness means that in order to know how new useful mutations behave in general, the only robust solution is to watch lots of new useful mutations in lots of otherwise identical populations.

The first clever thing about the project is that its authors knew in advance where to expect a beneficial mutation. Yeast cells reproduce both sexually and asexually—if the experimental populations are maintained in conditions that keep them reproducing asexually, mutations that turn off the costly cellular machinery necessary for sexual reproduction provide a measurable benefit.

By using a strain of yeast engineered to produce fluorescent protein in the course of sexual reproduction, the authors could check for the presence of permanently asexual mutants by taking a sample from the population, prompting it to mate and measuring the sample’s total fluorescence. Lower fluorescence would mean that more cells had lost the ability to reproduce sexually; if samples from a population were to become less and less fluorescent over time, the beneficial mutation would be spreading through the population.

Lang and his coauthors then set up the kind of experiment that you can only do with single-celled critters: they started 592 populations of yeast evolve for 1,000 generations of asexual reproduction. Each population started out from a single genetic strain, so differences between populations started from the same strain were purely due to differences in the random processes of mutation and drift. (The full experimental design used two different strains of yeast, and kept the population size at either 100,000 or 1,000,000 cells, for a total of four treatments.)

You might expect that the loss-of-sex mutation would reliably emerge and spread until it dominated each replicate population. In fact, that only occurred in a small fraction of the replicates. In many more cases, the loss-of-sex mutation showed up and started to spread, but was then overwhelmed by yeast that could still reproduce sexually—presumably because other, more beneficial mutations had arisen elsewhere in the population. This phenomenon, clonal interference, is widely expected to happen in competition among clonal strains.

What determined the success or failure of the loss-of-sex mutation? The authors found a considerable range of variation in the rate at which loss-of-sex strains increased in the experimental populations, suggesting that variation elsewhere in the genome contributed to the fitness of the yeast strain carrying the loss-of-sex mutation. Since every replicate population started as a genetically identical clone, that meant that mutations built up quite early in the course of experimental evolution. That variation corresponded to differences in the fitness of strains within the population—and the success or failure of the loss-of-sex mutation depended on whether it turned up in a strain that was already pretty fit to begin with.

Without recombination to mix up the genome, a beneficial mutation is bound to genetic variants at many, many other loci that may boost the benefits from that mutation, or cancel them out. In a clonal population, each genome succeeds or fails as a unit—a single useful mutation simply cannot do it alone.